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Cardiovascular Research 1995 30(5):663-667; doi:10.1016/S0008-6363(95)00077-1
© 1995 by European Society of Cardiology
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Copyright © 1995, European Society of Cardiology

Basilar arterial constriction caused by intracisternal NG-nitro-L-arginine in anesthetized monkeys

Tomio Okamura, Kazuhide Ayajiki and Noboru Toda*

Department of Pharmacology, Shiga University of Medical Science, Seta, Ohtsu 520-21, Japan

* Corresponding author. Tel.: (+81-775) 48-2181; Fax: (+81-775) 48-2183.

Objectives: The present study was designed to determine whether tonic nitric oxide (NO)-mediated vasodilator innervation participates in basilar arterial dilatation in the anesthetized Japanese monkey. Methods: The basilar arterial diameter was angiographically measured, and NG-nitro-L-arginine (L-NNA), a nitric oxide synthase inhibitor, was intracistemally applied. Results: The injection of L-NNA produced a sustained constriction of the basilar artery, the effect being reversed by the cisternal injection of L-arginine. The vasoconstriction tended to be accelerated by treatment with phentolamine. Under {alpha}-adrenoceptor blockade, hexamethonium significantly attenuated the vasoconstrictor response to L-NNA. Intracisternal injections of this inhibitor did not alter the systemic blood pressure and heart rate. Conclusions: These findings suggest that constriction by the NO synthase inhibitor of the monkey basilar artery is associated with suppression of synthesis of NO in vasodilator nerves receiving tonic impulses from the central nervous system. The basilar arterial tone appears to be regulated by nitroxidergic and adrenergic nerves and by NO derived from the endothelium in anesthetized monkeys.

KEYWORDS L-NAME; Monkey, anesthetized; Nitric oxide; Basilar artery; Arterial tone; EDRF


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